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At least 19 recordsLinked to original sources
PubMed1979

Plasma concentrations of pancuronium and neuromuscular blockade after injection into the isolated arm, bolus injection, and continuous infusion.

To establish whether the plasma concentration of pancuronium reflects magnitude of neuromuscular blockade, the authors determined times of recovery from neuromuscular blockade and associated plasma concentrations following equipotent doses of pancuronium using three methods of pancuronium administration: the isolated-arm technique in conscious volunteers (n = 4), and the bolus intravenous injection (n = 7) and continuous-infusion methods (n = 3) in anesthetized patients. Although maximum depressions of twitch tension were similar (85 +/- 11,91 +/- 6, and 92 +/- 4 per cent, respectively) with the three techniques, times to recovery from neuromuscular blockade differed significantly, being 10 +/- 2 min with the isolated-arm technique, 23 +/- 7 min with the bolus-injection technique, and 46 +/- 5 min with the continuous-infusion method. The plasma concentration of pancuronium necessary for neuromuscular blockade was least with the isolated-arm technique and greatest with continuous infusion. At 25 and 75 per cent recovery, mean plasma concentrations were 0.07 +/- 0.01 and 0.04 +/- 0.01 microgram/ml in the isolated arm; 0.13 +/- 0.04 and 0.09 +/- 0.02 microgram/ml after bolus injection, and 0.20 +/- 0.04 and 0.11 microgram/ml during continuous infusion, respectively. It is concluded that the relationship between plasma concentration of pancuronium and magnitude of neuromuscular blockade depends on the method of pancuronium administration.

Humans↗
PubMed1976

Mechaism of neuromuscular blockade with some antiepileptic drugs.

Effects of four antiepileptic drugs, viz., diphenylhydantoin, trimethadione, phenobarbitone and ethosuximide, were studied on different in vitro and in vivo skeletal muscle preparations which consisted of frog rectus, rat phrenic nerve diaphragm and cat gastrocnemius sciatic nerve preparations. A dose related blockade of neuromuscular transmission was seen with all the compounds tested. The blockade was mainly confined to the neuromuscular junction, although direct stimulation of muscle was slightly affected. The blockade was partially antagonized by physostigmine, adrenaline, succinylcholine, choline, tetraethylammonium and KCl and was additive to that due to tubocurarine. Moreover, the drugs were found to possess moderate local anaesthetic activity. The blockade was therefore considered to be partly due to curariform activity and partly due to their local anaesthetic activity.

Abdominal Muscles↗
PubMed1978

Effectiveness of pyridostigmine in reversing neuromuscular blockade produced by soman.

The effects of pyridostigmine pretreatment on the neuromuscular blockade produced by soman in anaesthetized, atropinized animals have been studied on the soleus and anterior tibialis muscle (rhesus monkeys, cats and rabbits) and the gastrocnemius muscle (guinea-pigs and rats). Pyridostigmine pretreatment produced a complete recovery of neuromuscular function following blockade by soman; the rate of recovery was similar in all the species, suggesting a common mechanism of action. In the absence of pyridostigmine or if pyridostigmine was delayed until after blockade by soman, there was no recovery of neuromuscular function. Detailed studies in the guinea-pig showed that the recovery of neuromuscular function was related to the dose of soman and to the degree of carbamoylation of blood cholinesterase at the time of nerve agent challenge, i.e. to the dose of pyridostigmine and the time interval between the administration of pyridostigmine and soman. It is suggested that the effectiveness of pyridostigmine pretreatment is due to the carbamoylation of a portion of the tissue acetylcholinesterase, which protects it against irreversible inhibition by soman: after poisoning spontaneous decarbamoylation produces sufficient free acetylcholinesterase to restore normal function.

Animals↗
PubMedDate not supplied

Neostigmine and 4-aminopyridine antagonism of lincomycin-pancuronium neuromuscular blockade in man.

Seven anesthetized patients were studied to determine the interaction between pancuronium and lincomycin and the ability of neostigmine and 4-aminopyridine to antagonize the block. Lincomycin 600 mg given IV alone did not decrease twitch tension. An 8 to 10% decrease in twitch tension occurred when lincomycin was given after neostigmine antagonism of pancuronium. Lincomycin augmented a partial pancuronium neuromuscular blockade. The combined lincomycin-pancuronium neuromuscular blockade was effectively antagonized by both neostigmine and 4-aminopyridine although the latter produced a slower rate of antagonism. The authros conclude that lincomycin, 600 mg IV, augments a pancuronium neurovascular blockade. 4-Aminopyridine offers no advantage over neostigmine and, in fact, may offer a disadvantage because of a slower rate of antagonism.

Adolescent↗
PubMed1979

Effects of neuromuscular blockade on respiratory mechanics in conscious man.

The effect of submaximal neuromuscular blockade (SMNB) on lung and chest wall mechanics was studied in six normal, awake subjects infused with pancuronium. Measurements of static lung volumes, specific airway conductance (sGaw), maximum expiratory and inspiratory flow-volume (MEFV, MIFV) curves, and static pressure-volume (PV) curves of the lung and of the relaxed chest wall were obtained after lung recoil pressure (Pst(L)) at full inflation had been reduced to 60 +/- 10% of control. Inspiratory capacity was decreased, but residual volume was not increased. Inspiratory PV curve of the lung was not modified, and the observed decrease in expiratory compliance and the slight increase in Pst(L) during deflation were compatible with the altered lung volume history. SMNB did not modify sGaw nor the relationship between Pst(L) and MEF; by contrast it markedly reduced MIF rates. Finally, SMNB transposed the chest wall PV curve to higher levels on the pressure axis (it decreased the outward pull of the chest wall) without greatly affecting its slope, and thereby it reduced the resting level of the respiratory system. We conclude that 1) muscle weakness per se does not affect the eleastic properties of the lungs and airways, and 2) involuntary respiratory muscle activity influences the elastic recoil of the chest wall. We believe this muscle activity originates from muscle spindles, and lies essentially in the inspiratory portion of the intercostal musculature.

Adult↗
PubMed1979

Prolongation of pancuronium-induced neuromuscular blockade by intravenous infusion of nitroglycerin.

Based upon clinical observation of undue prolongation of pancuronium-induced blockade in the presence of intravenous infusion of nitroglycerin, neuromuscular blockades produced by pancuronium, succinylcholine and d-tubocurarine were studied in 51 cats using the sciatic-gastrocnemius nerve-muscle preparation. Pancuronium-induced blockade was found to be significantly prolonged (P less than 0.1) in the presence of a nitroglycerin infusion of 1 microgram/kg/min (65 vs. 127 min). Less, but still significant, prolongation occurred when nitroglycerin, 0.5 microgram/kg/min, was infused. The intravenous infusion of nitroglycerin must be started prior to the pancuronium injection for the block to be prolonged. Neuromuscular blocks produced by succinylcholine and d-tubocurarine were not altered by nitroglycerin. In experiments using the isolated rat diaphragm preparation, the depth of pancuronium-induced block was found not to be changed by nitroglycerin, suggesting an effect of nitroglycerin on the process of recovery from blockade. These findings indicate a selective pancuronium-nitroglycerin interaction.

Animals↗
PubMed1979

Edrophonium antagonism of pancuronium-induced neuromuscular blockade in man: a reappraisal.

The ability of edrophonium to reverse the nondepolarizing neuromuscular blockade produced by pancuronium was studied in 40 adult patients during light nitrous oxide--enflurane anesthesia. Antagonism of paralysis was attempted when the train-of-four fade ratio had spontaneous recovered in various extents. Edrophonium was administered in incremental doses intravenously either until the fade ratio increased to 0.70 or more or until the total dose of drug amounted to 0.5 mg/kg. All patients who had spontaneous recovery of train-of-four fade ratios to at least 0.10 had adequate reversal with edrophonium. When the train-of-four count was three or fewer visible twitches, the response to endrophonium was unpredictable. No evidence of recurarization was seen.

Edrophonium↗
PubMed1978

Neuromuscular blockade of fazadinium bromide (AH 8165) in renal failure patients.

Fazadinium bromide (AH 8165) is a new non-depolarizing neuromuscular blocking agent with rapid onset of action and intermediate duration of effect. The characteristics of the neuromuscular blockade induced were compared in normal and renal failure patients by monitoring the mechanical responses of thumb adductor muscle to ulnar nerve stimulation. The data suggest that renal failure, even in anephric patients, does not influence the depth of neuromuscular relaxation when judged from the identical dose-effect curves in both groups of patients. Moreover, the duration of the neuromuscular block was not significantly increased in end-stage kidney failure patients, whether the initial or late phases of the spontaneous recovery of neuromuscular transmission were considered, and this occurred over the entire therapeutic range. However, additional incremental injections of fazadinium bromide should be used cautiously, as evidence appeared of prolonged duration of action. This agent, fazadinium bromide, may therefore present useful advantages to other non-depolarizing neuromuscular blocking agents as to clinical safety and effects in patients with renal insufficiency.

Adolescent↗
PubMedDate not supplied

Reversal of neuromuscular blockade by glycopyrrolate and neostigmine. A study of the effects on lower oesophageal sphincter tone.

The effect of intravenous glycopyrrolate and neostigmine, a drug combination routinely given to antagonize non-depolarising neuromuscular blockade, on lower oesophageal sphincter tone was studied in twenty patients undergoing Caesarean section. Glycopyrrolate 0.6 mg and neostigmine 2.5 mg i.v. increased LOS pressure insignificantly by a mean of 0.2 kPa (P less than 0.1). In contrast, glycopyrrolate 0.6 mg and neostigmine 5 mg increased LOS pressure by a mean of 1.2 kPa (P less than 0.001). The latter dosage of this drug combination thus appears preferable in patients presenting for emergency surgery, if the integrity of the lower oesophageal sphincter is to be maintained during extubation and recovery from general anaesthesia.

Anesthesia, Obstetrical↗
PubMed1975

Increased extrajunctional acetylcholine sensitivity produced by chronic acetylcholine sensitivity produced by chronic post-synaptic neuromuscular blockade.

1. Anaesthetized rats were paralysed for periods of up to 3 days by chronic administration of D-tubocurarine (DTC), succinylcholine or alpha-bungarotoxin. 2. After 3 days of treatment with DTC, the phrenic nerve remained active. Neuromuscular transmission and spontaneous miniature end-plate potentials (m.e.p.p.s) were restored after removal of the DTC. Resting potentials and input resistances of muscle fibres that had been paralysed for 3 days were similar to those in denervated fibers. 3. Chronic neuromuscular blockade increased the binding of [125-I]-alpha-bungarotoxin by extrajunctional regions of muscle. The time course of the increase was similar to that seen after denervation. Binding to muscles from animals that were anaesthetized and respirated, but not paralysed, was not increased. 4. Three days of paralysis increased the sensitivity of the extrajunctional muscle membrane to acetylcholine (ACh) applied by iontophoresis. 5. Approximately the same proportion of muscle fibres from muscles paralysed for 3 days gave overshooting action potentials in the presence of tetrodotoxin 10-minus 6 g/ml. as did fibres form muscles denervated for 3 days. 6. Chronic paralysis did not change the accumulation of acetylcholinesterase above a ligation in the sciatic nerve. 7. These results are consistent with the idea that extrajunctional ACh sensitivity is normally controlled by muscle activity.

Acetylcholine↗
PubMedDate not supplied

Amitriptyline therapy increases electrocardiographic changes during reversal of neuromuscular blockade.

Induction of anesthesia is associated with an increased incidence of cardiac arrhythmias in patients maintained on amitriptyline medication. This study presents additional evidence showing that, in experimental animals (cats), amitriptyline treatment also produces significant ST-T wave and conduction abnormalities during neostigmine reversal of neuromuscular blockade.

Amitriptyline↗
PubMed1975

Train-of-four nerve stimulation in the management of prolonged neuromuscular blockade following succinylcholine.

Four patients, all possessing an atypical form of plasma cholinesterase, developed prolonged paralysis following succinylcholine administration. The clinical management of all four cases was facilitated by monitoring the train-of-four stimulus. All patients showed marked "fade" of the train-of-four ratio, the initial ratios of the fourth to the first twitches being 50 per cent or less, indicating variable degrees of nondepolarizing neuromuscular blockade. Reversal of paralysis with anticholinesterase agents was completely successful in three cases, but only partially effective in the fourth because of the probable presence of a mixture of both depolarizing block and nondepolarizing block. In such a situation, caution in the interpretation of the train-of-four ratio is necessary, since this test measures only the nondepolarizing component of the block. Whether or not reversal with anticholinesterase drugs is attempted, clinical estimates of neuromuscular function, such as head lift, vital capacity, and inspiratory force, must be carefully correlated with train-of-four values. If reversal is attempted, the brief action of edrophonium provides a useful clinical trial.

Adolescent↗
PubMed1977

Neuromuscular blockade with anti-axoplasmic antibodies.

In the process of developing an immunopharmacologic method for identifying a "trophic" protein released from motor nerve terminals, a soluble fraction of peripheral nerve axoplasm was prepared. An attempt was made to eliminate contaminating myelin and basic protein. Antibodies were produced to soluble nerve proteins in all sheep immunized. On boosting, after a 6-week interval, the animals became weak, and some could not stand on the fifth day after injection. A distinct component of neuromuscular blockade was demonstrated electrically and in response to edrophonium. Because this syndrome was (1) in the broadest sense, an experimental allergic neuropathy but produced by a distinctly different antigen than has been utilized previously (the soluble nerve proteins represented the axoplasmic compartment) and (2) a clinical condition associated with a defect in neuromuscular transmission, this may represent a new and potentially important model in the study of neuromuscular and other neurologic diseases.

Animals↗
PubMed1976

Comparative evaluation of neuromuscular blockade and reversibility of AH 8165 and pancuronium bromide in man.

The neuromuscular properties of AH 8165 were compared to those of pancuronium bromide in 66 patients during analgesic anesthesia procedures. Administration of 0.5 mg/kg AH 8165 and 0.04 mg/kg pancuronium bromide produced very similar degrees of non-depolarizing block. AH 8165 acted quicker and therefore gave better conditions for intubation. Spontaneous recovery of muscle twitch tension was slightly shorter for AH 8165 than for pancuronium bromide, whether small or larger amounts of drugs were used. Administration of neostigmine caused rapid and complete return of muscle twitch tension, well-maintained tetanus and insignificant posttetanic potentiation within 20 minutes, with a similar efficiency of competitive neuromuscular block reversal for both drugs.

Adult↗
PubMedDate not supplied

"Twitch box": a new device to monitor neuromuscular blockade.

It is proposed that this "twitch box" be used whenever monitoring of neuromuscular transmission is indicated, since it is simple to use under clinical conditions, does not require critical placement or adjustment of the hand, produces quantitative information comparable to the force transducer, and is safe.

Humans↗